EXPRESSION OF COMPLEMENT RECEPTORS AND REGULATORY PROTEINS ON ALVEOLAR CD4-1 INFECTED INDIVIDUALS( LYMPHOCYTES FROM HUMAN IMMUNODEFICIENCY VIRUS)

Several lines of evidence suggest a dysregulation of the complement sy stem in human immunodeficiency virus-1 (HIV-1) infected patients. The aim of this study was to elucidate whether CD4+ alveolar lymphocytes f rom HIV-1 infected patients show a loss of complement regulatory prote ins that would render these cells susceptible to antibody-dependent co mplement-mediated cytotoxicity. We investigated the expression of comp lement regulatory (CD46, CD55, CD59) and complement receptor (CRI, CR2 , CR3, CR4) proteins on alveolar cells by flow cytometry. Cells were o btained by bronchoalveolar lavage from 17 HIV-1 infected and 12 HIV-I negative individuals. Expression of adhesion molecules (leucocyte func tional associated antigen-1 (LFA-1), intercellular adhesion molecule-1 (ICAM-1)) and CD30 were evaluated in patient subgroups. In addition, interleukin (IL)-1 beta, tumour necrosis factor alpha (TNF-alpha), IL- 4 and interferon gamma (IFN-gamma) concentrations were measured in sup ernatants of alveolar cells. We found a significantly reduced expressi on of CD46 and CD59 on CD4+ alveolar lymphocytes from HIV-1 infected i ndividuals, whereas the expression of CR3, CR4, ICAM-1 and CD30 was in creased. IL-1 beta and TNF-alpha concentration in supernatants of alve olar cells was augmented in HIV-1 infected patients, but did not corre late with the expression of surface molecules. IFN-gamma concentration was also increased and showed an inverse relationship to the surface expression of CD30 on CD4+. Our data suggest that in human immunodefic iency virus-1 infection an increased level of activation is associated with a diminished expression of complement regulatory proteins on CD4 + alveolar lymphocytes. This phenomenon might contribute to the deplet ion of CD4+ lymphocytes and the local immunodeficiency in the pulmonar y compartment.